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Persistent hepatitis D virus mono-infection in humanized mice is efficiently converted by hepatitis B virus to a productive co-infection

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Persistent hepatitis D virus mono-infection in humanized mice is efficiently converted by hepatitis B virus to a productive co-infection. / Giersch, Katja; Helbig, Martina; Volz, Tassilo; Allweiss, Lena; Mancke, Lisa; Lohse, Ansgar W; Polywka, Susanne; Pollok, Jörg M; Petersen, Jörg; Taylor, John; Dandri, Maura; Lütgehetmann, Marc.

In: J HEPATOL, Vol. 60, No. 3, 01.03.2014, p. 538-44.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Giersch, K, Helbig, M, Volz, T, Allweiss, L, Mancke, L, Lohse, AW, Polywka, S, Pollok, JM, Petersen, J, Taylor, J, Dandri, M & Lütgehetmann, M 2014, 'Persistent hepatitis D virus mono-infection in humanized mice is efficiently converted by hepatitis B virus to a productive co-infection', J HEPATOL, vol. 60, no. 3, pp. 538-44. https://doi.org/10.1016/j.jhep.2013.11.010

APA

Giersch, K., Helbig, M., Volz, T., Allweiss, L., Mancke, L., Lohse, A. W., Polywka, S., Pollok, J. M., Petersen, J., Taylor, J., Dandri, M., & Lütgehetmann, M. (2014). Persistent hepatitis D virus mono-infection in humanized mice is efficiently converted by hepatitis B virus to a productive co-infection. J HEPATOL, 60(3), 538-44. https://doi.org/10.1016/j.jhep.2013.11.010

Vancouver

Giersch K, Helbig M, Volz T, Allweiss L, Mancke L, Lohse AW et al. Persistent hepatitis D virus mono-infection in humanized mice is efficiently converted by hepatitis B virus to a productive co-infection. J HEPATOL. 2014 Mar 1;60(3):538-44. https://doi.org/10.1016/j.jhep.2013.11.010

Bibtex

@article{a1190eacac094084a3a07303ad25382d,
title = "Persistent hepatitis D virus mono-infection in humanized mice is efficiently converted by hepatitis B virus to a productive co-infection",
abstract = "BACKGROUND & AIMS: Clinical studies have shown that hepatitis delta virus (HDV) infection can persist for years and intrahepatic latency of the large delta antigen (HDAg) has been detected following liver transplantation. However, large HDAg arising via RNA-editing is associated with increasing amounts of non-infectious HDV quasi-species. This study investigated whether HDV could persist intrahepatically in the absence of HBV in vivo and whether infectious HDV could subsequently be released following HBV super-infection.METHODS: Humanized mice were infected with HDV particles lacking HBV. To test for rescue of latent HDV infection 3 and 6 weeks HDV mono-infected mice were super-infected with HBV. Viral loads and cell toxicity were determined by qRT-PCR and immunohistochemistry.RESULTS: The presence of HDAg-positive human hepatocytes determined after 2, 3, and 6 weeks of HDV inoculation demonstrated establishment and maintenance of intrahepatic HDV mono-infection. Although intrahepatic amounts of large HDAg and edited HDV RNA forms increased over time in HDV mono-infected livers, HBV super-infection led to prompt viremia development (up to 10(8) HDV RNA and 10(7) HBV-DNA copies/ml) even after 6 weeks of latent mono-infection. Concurrently, the number of HDAg-positive human hepatocytes increased, demonstrating intrahepatic HDV spreading. The infectivity of the rescued HDV virions was verified by serial passage in naive chimeric mice.CONCLUSIONS: HDV mono-infection can persist intrahepatically for at least 6 weeks before being rescued by HBV. Conversion of a latent HDV infection to a productive HBV/HDV co-infection may contribute to HDV persistence even in patients with low HBV replication and in the setting of liver transplantation.",
author = "Katja Giersch and Martina Helbig and Tassilo Volz and Lena Allweiss and Lisa Mancke and Lohse, {Ansgar W} and Susanne Polywka and Pollok, {J{\"o}rg M} and J{\"o}rg Petersen and John Taylor and Maura Dandri and Marc L{\"u}tgehetmann",
note = "Copyright {\textcopyright} 2013 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.",
year = "2014",
month = mar,
day = "1",
doi = "10.1016/j.jhep.2013.11.010",
language = "English",
volume = "60",
pages = "538--44",
journal = "J HEPATOL",
issn = "0168-8278",
publisher = "Elsevier",
number = "3",

}

RIS

TY - JOUR

T1 - Persistent hepatitis D virus mono-infection in humanized mice is efficiently converted by hepatitis B virus to a productive co-infection

AU - Giersch, Katja

AU - Helbig, Martina

AU - Volz, Tassilo

AU - Allweiss, Lena

AU - Mancke, Lisa

AU - Lohse, Ansgar W

AU - Polywka, Susanne

AU - Pollok, Jörg M

AU - Petersen, Jörg

AU - Taylor, John

AU - Dandri, Maura

AU - Lütgehetmann, Marc

N1 - Copyright © 2013 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

PY - 2014/3/1

Y1 - 2014/3/1

N2 - BACKGROUND & AIMS: Clinical studies have shown that hepatitis delta virus (HDV) infection can persist for years and intrahepatic latency of the large delta antigen (HDAg) has been detected following liver transplantation. However, large HDAg arising via RNA-editing is associated with increasing amounts of non-infectious HDV quasi-species. This study investigated whether HDV could persist intrahepatically in the absence of HBV in vivo and whether infectious HDV could subsequently be released following HBV super-infection.METHODS: Humanized mice were infected with HDV particles lacking HBV. To test for rescue of latent HDV infection 3 and 6 weeks HDV mono-infected mice were super-infected with HBV. Viral loads and cell toxicity were determined by qRT-PCR and immunohistochemistry.RESULTS: The presence of HDAg-positive human hepatocytes determined after 2, 3, and 6 weeks of HDV inoculation demonstrated establishment and maintenance of intrahepatic HDV mono-infection. Although intrahepatic amounts of large HDAg and edited HDV RNA forms increased over time in HDV mono-infected livers, HBV super-infection led to prompt viremia development (up to 10(8) HDV RNA and 10(7) HBV-DNA copies/ml) even after 6 weeks of latent mono-infection. Concurrently, the number of HDAg-positive human hepatocytes increased, demonstrating intrahepatic HDV spreading. The infectivity of the rescued HDV virions was verified by serial passage in naive chimeric mice.CONCLUSIONS: HDV mono-infection can persist intrahepatically for at least 6 weeks before being rescued by HBV. Conversion of a latent HDV infection to a productive HBV/HDV co-infection may contribute to HDV persistence even in patients with low HBV replication and in the setting of liver transplantation.

AB - BACKGROUND & AIMS: Clinical studies have shown that hepatitis delta virus (HDV) infection can persist for years and intrahepatic latency of the large delta antigen (HDAg) has been detected following liver transplantation. However, large HDAg arising via RNA-editing is associated with increasing amounts of non-infectious HDV quasi-species. This study investigated whether HDV could persist intrahepatically in the absence of HBV in vivo and whether infectious HDV could subsequently be released following HBV super-infection.METHODS: Humanized mice were infected with HDV particles lacking HBV. To test for rescue of latent HDV infection 3 and 6 weeks HDV mono-infected mice were super-infected with HBV. Viral loads and cell toxicity were determined by qRT-PCR and immunohistochemistry.RESULTS: The presence of HDAg-positive human hepatocytes determined after 2, 3, and 6 weeks of HDV inoculation demonstrated establishment and maintenance of intrahepatic HDV mono-infection. Although intrahepatic amounts of large HDAg and edited HDV RNA forms increased over time in HDV mono-infected livers, HBV super-infection led to prompt viremia development (up to 10(8) HDV RNA and 10(7) HBV-DNA copies/ml) even after 6 weeks of latent mono-infection. Concurrently, the number of HDAg-positive human hepatocytes increased, demonstrating intrahepatic HDV spreading. The infectivity of the rescued HDV virions was verified by serial passage in naive chimeric mice.CONCLUSIONS: HDV mono-infection can persist intrahepatically for at least 6 weeks before being rescued by HBV. Conversion of a latent HDV infection to a productive HBV/HDV co-infection may contribute to HDV persistence even in patients with low HBV replication and in the setting of liver transplantation.

U2 - 10.1016/j.jhep.2013.11.010

DO - 10.1016/j.jhep.2013.11.010

M3 - SCORING: Journal article

C2 - 24280293

VL - 60

SP - 538

EP - 544

JO - J HEPATOL

JF - J HEPATOL

SN - 0168-8278

IS - 3

ER -